1. Field of the Invention
The present invention relates to a novel DNA whose expression level fluctuates in leukocytes of IgA nephropathy patients in comparison with leukocytes of healthy persons, a process for isolating the DNA, a novel protein encoded by the DNA, an antibody recognizing the protein, a method for detecting the protein or the DNA, and methods of diagnosis and treatment of IgA nephropathy.
2. Brief Description of the Background Art
IgA nephropathy is a chronic glomerulonephritis which is characterized in that an IgA immune complex considered to be derived from blood deposits in glomerulus of the kidney. In Japan, the IgA nephropathy occupies 30% or more of primary renal diseases, having the highest frequency as a single renal disease, and 15 to 30% of the disease becomes renal failure due to poor prognosis. However, since the cause of the disease of IgA nephropathy is still unclear, a fundamental therapeutic method has not been found. Additionally, definite diagnosis of IgA nephropathy imposes heavy burden on patients, because the method is carried out by taking out a portion of the kidney by biopsy and recognizing deposition of the IgA immune complex in mesangium by means of immunological staining.
It has been reported that about 50% of the patients with IgA nephropathy have a high blood IgA level [Diseases of the Kidney, 5th edition (1993), Nephron, 29, 170 (1981)]. It is considered that B cells relate to the production of IgA in blood and T cells relate to the regulation of the production. Furthermore, it has been reported that the production of cytokine, such as interleukin 4, interleukin 5, interleukin 6 or TGF-β (transforming growth factor-β), is high in peripheral T cells of IgA nephropathy patients in comparison with healthy persons [Clinical & Experimental Immunology, 103, 125 (1996), Kidney International, 46, 862 (1994)] and that integrin, such as VLA (very late activation)-4 and VLA-5, are strongly activated in peripheral lymphocytes of IgA nephropathy patients [Nephrology, Dialysis, Transplantation, 10, 1342 (1995)]. On the basis of these facts, it is considered that, in IgA nephropathy, the production of IgA becomes excess due to abnormality in the immune system, the resulting IgA immune complex in blood deposits on the glomerulus, and activation of the complement system caused thereby and the like exert influence upon disorders of the glomerulus, but the cause of IgA nephropathy has not been reported.